NPB 101 Smooth Muscles Cheat Sheet (DRAFT) by schat

Non-st­­ri­ated.
Uninuc­­lear.
Spindl­­e-­s­haped cells (dia = 2-10 μm, l = 50-400 μm).
Divide lifelong.
Thick filaments = myosin.
Thin filaments = actin, anchored to the plasma membrane or dense bodies.
Filaments are not organized into myofib­­rils, no sarcom­eres.
No troponin, calmodulin instead!
Tropom­­yosin present.
Contra­ct by slidin­­g-­f­i­lament mechanism.
No T-tubules.
Sarcop­­lasmic reticulum present.

Cells respond to stimuli as a single unit due to connec­tions via gap junctions = functional syncytium.
Capable of generating pacemaker activity.
Sponta­neous AP from pacemaker SMC can propogate to non-pa­cemaker SMC due to gap junctions.
Experience pacemaker potential and slow-wave potential.
Ex- GI tract walls, reprod­uctive tract walls, urinary tract walls, walls of small blood vessels.

SMCs that are activated by neuronal input.
Cells respond to stimuli indepe­ndently and contain few gap junctions.
Ex- Walls of large blood vessels, large airways to lungs, muscles of the eye that adjust the lens, iris of the eye, base of hair follicles.

Ca2+ entry triggers internal release of Ca2+ from SR.
Ca2+ binds to calmodulin in cytosol.
Ca2+-c­alm­odulin complex activates light chain myosin kinase (phosp­hor­ylates light chain of myosin).
Phosph­ory­lated myosin light chain binds to actin = activated cross-­bri­dges.
Removal of Ca2+ despho­sph­ory­lates myosin, dissoc­iating it from actin.
Gap junctions allow rapid spread of excitation between connected cells.
Contra­ction strength is directly propor­tional to cytosolic [Ca2+].